Genetic determination of sleep EEG profiles in healthy humans

Landolt, Hans‐Peter

doi:10.1016/b978-0-444-53839-0.00004-1

Cited by 62 publications

(48 citation statements)

References 39 publications

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“…Human sleep and particularly oscillatory EEG activity during sleep is highly heritable and very stable within individuals (689). In addition, large interindividual differences in the sleep EEG exist, which are more than 10 times higher than those, observed within subjects across multiple nights of sleep.…”

Section: Stability and Heritability Of Sleepmentioning

confidence: 99%

About Sleep's Role in Memory

Rasch

Born

2013

Physiological Reviews

2,265

2,026

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Over more than a century of research has established the fact that sleep benefits the retention of memory. In this review we aim to comprehensively cover the field of "sleep and memory" research by providing a historical perspective on concepts and a discussion of more recent key findings. Whereas initial theories posed a passive role for sleep enhancing memories by protecting them from interfering stimuli, current theories highlight an active role for sleep in which memories undergo a process of system consolidation during sleep. Whereas older research concentrated on the role of rapid-eye-movement (REM) sleep, recent work has revealed the importance of slow-wave sleep (SWS) for memory consolidation and also enlightened some of the underlying electrophysiological, neurochemical, and genetic mechanisms, as well as developmental aspects in these processes. Specifically, newer findings characterize sleep as a brain state optimizing memory consolidation, in opposition to the waking brain being optimized for encoding of memories. Consolidation originates from reactivation of recently encoded neuronal memory representations, which occur during SWS and transform respective representations for integration into long-term memory. Ensuing REM sleep may stabilize transformed memories. While elaborated with respect to hippocampus-dependent memories, the concept of an active redistribution of memory representations from networks serving as temporary store into long-term stores might hold also for non-hippocampus-dependent memory, and even for nonneuronal, i.e., immunological memories, giving rise to the idea that the offline consolidation of memory during sleep represents a principle of long-term memory formation established in quite different physiological systems.

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Section: Stability and Heritability Of Sleepmentioning

confidence: 99%

About Sleep's Role in Memory

Rasch

Born

2013

Physiological Reviews

2,265

2,026

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“…Despite this, little is known about the genetic underpinnings of sleep spindles. Genome-wide association studies (GWAS) have been conducted for sleep disorders (132), sleep duration (133) and insomnia (134), but genetic studies of the sleep EEG used relatively small samples and only a few candidate genes (135). To understand genetic contributions to spindle deficits in SZ, it is important to conduct well-powered genetic studies of spindles in humans.…”

Section: Genetic Mechanisms Of Sleep Spindlesmentioning

confidence: 99%

Reduced Sleep Spindles in Schizophrenia: A Treatable Endophenotype That Links Risk Genes to Impaired Cognition?

Manoach

Pan

Purcell

et al. 2016

Biological Psychiatry

190

155

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Although schizophrenia is defined by waking phenomena, abnormal sleep is a common feature. In particular, there is accumulating evidence of a sleep spindle deficit. Sleep spindles, a defining thalamocortical oscillation of non-rapid eye movement Stage 2 sleep, correlate with IQ and are thought to promote long-term potentiation and enhance memory consolidation. Here we review evidence that reduced spindle activity in schizophrenia is an endophenotype that impairs sleep-dependent memory consolidation, contributes to symptoms and is a novel treatment biomarker. Studies showing that spindles can be pharmacologically enhanced in schizophrenia and that increasing spindles improves memory in healthy individuals suggest that treating spindle deficits in schizophrenia may improve cognition. Spindle activity is highly heritable and recent large-scale genome-wide association studies have identified schizophrenia risk genes that may contribute to spindle deficits and illuminate their mechanisms. For example, the schizophrenia risk gene CACNA1I encodes a calcium channel that is abundantly expressed in the thalamic spindle generator and plays a critical role in spindle activity in a mouse knockout. Future genetic studies of animals and humans can delineate the role of this and other genes in spindles. Such cross-disciplinary research, by forging empirical links in causal chains from risk genes to proteins and cellular functions, through to endophenotypes, cognitive impairments, symptoms and diagnosis, has the potential to advance the mechanistic understanding, treatment and prevention of schizophrenia. This review highlights the importance of deficient sleep-dependent memory consolidation among the cognitive deficits of schizophrenia and implicates reduced sleep spindles as a potentially treatable mechanism.

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“…The mechanisms underlying this hourglass-like process are still debated, but animal research suggests that it arises from a use-dependent local augmentation of sleep-promoting substances (adenosine (Basheer et al, 2004) and cytokines (Krueger, 2008)), from an increase in extracellular glutamate level (Dash et al, 2009), and/or from an experience-dependent increase of average brain synaptic strength, excitability and size during wakefulness (Vyazovskiy et al, 2008; Bushey et al, 2011). Other molecular markers of sleep loss have been identified in rodents (Franken and Dijk, 2009), while human polymorphisms have been associated with difference in sleep regulation [e.g., PERIOD3 (PER3) (Viola et al, 2007) , Adenosine Deaminase (ADA) , Adenosin A2a receptor (ADORA2A), Brain Derived Neurotrophic Factor (BDNF), Catechol-O-Methyltransferase (COMT) , human leukocyte antigen (HLA) , (Goel and Dinges, 2011), dopamine transporter (DA) , (Valomon et al, 2014), ABCC9 (Allebrandt et al, 2013); for review see (Landolt, 2011)]. At the macroscopic scale, the electroencephalogram (EEG) provides the best established markers of sleep need and intensity: slow wave activity (SWA; 0.5–4 Hz) during Non-Rapid Eye Movement (NREM) sleep (Dijk et al, 1987, 1997), and theta activity (4–8 Hz) during wakefulness (Cajochen et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Neuroimaging, cognition, light and circadian rhythms

Gaggioni¹,

Maquet²,

Schmidt³

et al. 2014

Front. Syst. Neurosci.

107

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In humans, sleep and wakefulness and the associated cognitive processes are regulated through interactions between sleep homeostasis and the circadian system. Chronic disruption of sleep and circadian rhythmicity is common in our society and there is a need for a better understanding of the brain mechanisms regulating sleep, wakefulness and associated cognitive processes. This review summarizes recent investigations which provide first neural correlates of the combined influence of sleep homeostasis and circadian rhythmicity on cognitive brain activity. Markers of interindividual variations in sleep-wake regulation, such as chronotype and polymorphisms in sleep and clock genes, are associated with changes in cognitive brain responses in subcortical and cortical areas in response to manipulations of the sleep-wake cycle. This review also includes recent data showing that cognitive brain activity is regulated by light, which is a powerful modulator of cognition and alertness and also directly impacts sleep and circadian rhythmicity. The effect of light varied with age, psychiatric status, PERIOD3 genotype and changes in sleep homeostasis and circadian phase. These data provide new insights into the contribution of demographic characteristics, the sleep-wake cycle, circadian rhythmicity and light to brain functioning.

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Genetic determination of sleep EEG profiles in healthy humans

Cited by 62 publications

References 39 publications

About Sleep's Role in Memory

About Sleep's Role in Memory

Reduced Sleep Spindles in Schizophrenia: A Treatable Endophenotype That Links Risk Genes to Impaired Cognition?

Neuroimaging, cognition, light and circadian rhythms

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